Lumbar spinal stenosis

INTRODUCTION

Lumbar spinal stenosis may be congenital or acquired. A classic clinical presentation is described as neurogenic claudication. Physical signs of sensory loss, weakness, and attenuation of reflexes often are mild and limited in distribution. Neuroimaging of the lumbosacral spine with MRI and electrodiagnostic (electromyographic [EMG]) tests are the most informative diagnostic modalities. Conservative management often is successful, but surgical decompression may be indicated in refractory cases.

Lumbar spinal stenosis perhaps is understood best as a clinicopathologic disorder: narrowing of the lumbar spinal canal and the nerve root canals (causing central and lateral recess stenosis, respectively) typically is brought about by the process of osteoarthritis and leads to compression of the contents of the canals—the neural and vascular structures, causing neurologic symptoms (typically low back and leg pain and lower limb numbness and weakness) that are intermittent, characteristically triggered by ambulation (ameliorated by pausing), and generally positional (aggravated by standing and eased by trunk flexion). The emergence of spinal stenosis as a recognizable disease entity took a major step forward in 1954 with the work of the Dutch neurosurgeon, H. Verbiest [1] (described in a literature review by Javid and Hadar [2]), who coined the term, “stenosis of the vertebral canal,” and defined the pathologic changes that take place in the lumbar spinal canal engendered by encroachment of the canal contents by hypertrophied articular processes. Although having a narrow lumbar spinal canal is a necessary component of the condition, alone it is not sufficient for the disorder to be expressed, because this requires a degree of narrowing that compresses canal contents and causes compromise in sensory and motor nerve function. Accordingly, there may be a poor correlation between “stenosis” demonstrated by neuroimaging methods and clinical symptoms [3]. As Haig and colleagues [4] point out, there is no criterion standard for the clinical diagnosis of lumbar spinal stenosis. Clinically, the constellation of symptoms not always is classic; radiologically, there is no clear relationship between the severity of symptoms and degree of stenosis; and electrophysiologically, there is no predictable, specific electromyographic (EMG) abnormality.

Lumbar spinal stenosis is a common problem in adult life. It is estimated to be present in 5 of every 1000 Americans over age 50 [5]. It accounts for 5% of patients who present with persistent low back pain to a general physician and up to 14% of patients who seek the opinion of a specialist [6]. It is the leading preoperative diagnosis for adults older than age 65 who undergo spine surgery [7]; in the United States, rates of surgery for spinal stenosis increased eightfold from 1979 to 1992 in patients over age 65 [8]. It commonly affects adults in their sixth and seventh decades when it most likely is a result of acquired degenerative joint disease—lumbar spondylosis. A subset of adults in their third and fourth decades also is affected, and these individuals typically have congenital narrowing of the lumbosacral spine (discussed later) [9]. Some patients who have the congenital form of spinal stenosis have achondroplastic dwarfism and at age 38 have a relatively young mean age of presentation, attesting to the primary nature of the stenosis [10].

  • Clinical features

Patients present with the insidious onset of diffuse, often symmetric symptoms, reflecting the bilateral nature of the underlying disease process that often involves several vertebral levels [11]. The first symptoms of lumbar spinal stenosis frequently are low back pain and morning stiffness relieved by activity [12]. As time passes, there frequently is low back, buttock, thigh, and calf discomfort, often described as a cramping, burning sensation, sometimes with associated numbness and tingling in the legs and thighs. Weakness is not a prominent symptom but may be present, most often manifested as partial foot drop or weakness in plantar flexion, especially after prolonged standing or walking, and pointing to the common involvement of muscles served by L5 and S1 roots [13]. A characteristic of the symptoms produced by lumbar spinal stenosis is that they are induced or triggered by standing and walking (activities that extend the lumbar spine) and eased by sitting or flexing the trunk. The latency from the start of standing to the onset of pain varies from patient to patient and also changes over time for individual patients, becoming shorter when and if the disease process evolves. A classic clinical feature of lumbar canal stenosis is neurogenic claudication, the dynamic phenomenon of standing- and walking-related symptoms (thigh or leg pain preceding numbness and motor weakness), causing patients to limp and then to cease the provocative activity [14]. It is to be distinguished from the vascular mechanism encountered more commonly underlying painful legs, induced by walking, in the context of atherosclerotic peripheral vascular disease. In this vascular disorder, the typical history is that cramping develops in the calves with activity (such as walking, cycling, or descending, and especially ascending, stairs) and that relief is obtained by sitting and resting. In neurogenic claudication, by contrast, ascending stairs typically is less likely to induce symptoms than descending, probably because the former allows for a partially flexed trunk, whereas in the latter, the lumbar spine straightens out, obliging patients to walk downstairs backward to adopt a forward-flexed position [5]; cycling is tolerated much more than walking. Patients who have lumbar spinal stenosis typically are fairly comfortable on shopping outings if they can lean over while pushing a grocery cart.

In the early stages of the disorder, the symptoms may be mild and provoked after an extended period of standing or walking, but as time passes, the disease seems to enter an extended plateau phase in many patients. In others, symptoms may become more pronounced and diffuse, triggered by only brief periods of standing, reaching the point where quality of life may become seriously compromised. In these advanced cases, patients barely are able to walk short distances without severe symptoms and reflexively attempt to attenuate any discomfort by using a stooped or anthropoid posture (effectively flexing the back) that presumably allows for widening of the lumbar spinal canal [15]. In approximately 10% of patients, generally those who have the most advanced degrees of lumbar spinal stenosis, there are symptoms of bladder control difficulties, manifested as recurrent urinary tract infections associated with an atonic bladder, incontinence, and, rarely, episodes of urinary retention [9].

The examination findings are muted, in contrast to the findings in lumbosacral radiculopathy (which may coexist with lumbar spinal stenosis). In lumbosacral radiculopathy, there is straight leg raising and reverse straight leg raising positivity, segmental weakness, attenuation of reflex activity, and dermatomal sensory loss. In lumbar spinal stenosis, there may be flattening of the lumbar lordosis and a decrease in lumbar extension. Positive straight leg raising—complaints of a severe sciatica-like pain in a raised leg at 30° to 40° of elevation—is uncommon in patients who have lumbar spinal stenosis [15]. Provocative measures suggestive of lumbar spinal stenosis include lying prone in lumbar hyperextension, walking, and walking with an exaggerated lumbar lordosis until symptoms appear, followed by relief of symptoms by leaning forward [7]. At rest there may be a paucity of findings [14], but with onset of symptoms after walking or extending the spine, there may be diminution in patellar and Achilles tendon reflexes, mild sensory loss in L4 to S1 dermatomes, and mild weakness in L4-, L5- and S1-innervated muscles—hence, the importance of the sage advice from Alvarez and Hardy [15] to perform a neurologic examination before and immediately after symptoms appear after a short period of ambulation.

Finally, it is important to assess patients for clinical evidence of vascular disease, which, as discussed previously, might simulate some of the symptoms of lumbar spinal stenosis, notably claudication. The examination includes the evaluation of skin color, turgor, and temperature; distal lower limb pulses; and auscultation for arterial bruits. Absence of clinical features of peripheral vascular disease should heighten confidence in a diagnosis of lumbar spinal stenosis [7].

  • Anatomy and pathology

The spinal cord in adults ends at the upper border of the L1 vertebral body and continues as multiple nerve roots, the cauda equina, that descend to their specific neural foramena, providing exit from the lumbosacral spinal canal. The spinal canal ranges from 15 to 23 mm in its anteroposterior diameter and is a triangular space bounded anteriorly by the dorsal surfaces of the bodies of the lumbar vertebrae and the disk spaces (covered by the posterior longitudinal ligament), medially by the pedicles that extend from the lateral margin of the vertebral body, posteriorly by the laminae of the vertebral arch and their covering, the ligamentum flavum; and the facet joints that are part of the posterior elements of each vertebral body [7], [11], [15]. The vertebral bodies are connected to each other by the disks anteriorly and two facet or zygoapophyseal joints posteriorly. The disks are composed of a tough outer connective tissue annulus fibrosis and a soft, jelly-like center, the nucleus pulposus.

There are two major categories of lumbar spinal stenosis: congenital and acquired. The major contributors to narrowed lumbar canals on a congenital basis are short pedicles, thickened lamina and facets, and excessive scoliotic or lordotic curves [15]. Patients who have these congenital anatomic changes have a small safety factor for the emergence of clinically significant lumbar spinal stenosis, which may be precipitated by further canal narrowing from later life–onset superimposed degenerative joint changes. Defects in cellular metabolism leading to retardation of cartilaginous growth and irregular intracartilagenous bone formation lead to congenital spinal stenosis in achondroplastic dwarfism, where there is significant narrowing of the spinal canal in all its dimensions, especially in the upper lumbar regions because of shortened pedicles, hypertrophied zygapophyseal joints, and thickened laminae [10].

The majority of cases of lumbar spinal stenosis, however, are acquired, and stem from degenerative or arthritic changes that affect the three-joint complex between lumbar vertebrae: the two zygoapophyseal (facet) joints posteriorly and the adjoining intervertebral disk anteriorly [9]. The degenerative process begins most often with the disk and affects the articular processes secondarily. Initially, there is desiccation of the disk, narrowing of the disk space, rents or fissures in the annulus, disk bulging, and frank herniation of nucleus pulposus. This soon is followed by hypertrophic degenerative changes of the facets (osteophyte formation) and thickening of the ligamentum flavum. This results in central narrowing, so that the anteroposterior diameter is attenuated (typically to less than 12 mm) [7], with compression of the cauda equina, and lateral narrowing (at the recesses), with root compression at the entrance of the intervertebral foramen. Spondylolysis (a defect in the pedicles, the pars interarticularis—congenital or acquired) may lead to spondylolisthesis, the anterior displacement of one vertebra relative to the one beneath it, further narrowing an already stenotic lumbar canal [16].

The spine is the site affected second most commonly in Paget’s disease, predisposing patients to spinal stenosis, occurring in one third of those who have spinal involvement [17]. Pagetic spinal stenosis is brought about by bone remodeling of lumbar vertebrae, with bone expansion in all directions: posteriorly from the vertebral bodies, anterioromedially from the vertebral lamina, and medially from the pedicles. This leads to hypertrophic facet arthropathy and resulting spinal stenosis. Some cases of neurologic deterioration do not result from direct compression of neural elements, rather from spinal ischemia resulting from diversion of blood flow through remodeled hypervascular pagetic bone (referred to as the arterial steal phenomenon) [17].

  • Pathogenesis

Three explanations are advanced to explain the phenomenon of neurogenic claudication, the cardinal manifestation of lumbar spinal stenosis. They are designated the postural, the ischemic, and the venous stasis (stagnant hypoxia) theories [9]. The postural theory suggests that symptoms are explained by transient compression of the cauda equina (leading to sensory and motor axon dysfunction) by degenerated intervertebral disks and thickened ligamenta flava, when the lumbar spine is extended and lordosis is accentuated, either at rest or in the erect posture [15]. In the ischemic theory, it is proposed that the metabolic demand of the cauda equina cannot be met during activity (eg, walking), that blood flow needs of the lumbosacral nerve roots are not met by the local vasculature that is compromised by lumbar spinal stenosis. Porter [16] suggested the venous stasis theory: that the underlying mechanism of neurogenic claudication is inadequate oxygenation or the accumulation of metabolites in the cauda equina. He presented evidence from a porcine model that venous pooling of one or more nerve roots of the cauda equina between two levels of low pressure stenosis transitions to venous engorgement during exercise (walking), that in turn tends to prevent the expected arteriolar vasodilation response to activity, leading to nerve conduction failure with resulting symptoms of tiredness, weakness, and discomfort in the legs when walking.

  • Diagnostic testing

Standing center stage among diagnostic testing modalities in the evaluation of patients suspected of having lumbar spinal stenosis is neuroimaging with MRI. This noninvasive test with its multiplanar imaging capability provides the most complete assessment of the anatomy of the lumbosacral spine and allows adequate visualization of the spinal cord, cauda equina, and exiting nerve roots and their relationships to the various elements that comprise the spinal canal, including the ligaments, epidural fat, subarachnoid space, and intervertebral disks, with excellent detail [7], [15]. A variety of MRI sequences with gadolinium also reveals pathology of the vertebrae, the spinal canal, and the cauda equina that might mimic the clinical features of lumbar spinal stenosis—for example, infectious or neoplastic processes (see differential diagnosis discussion). If for any reason MRI cannot be performed (eg, contraindicated because the subject has a cardiac pacemaker), CT myelography provides appropriate alternative imaging resolution and reveals spinal canal pathology clearly.

Electrodiagnostic studies are helpful in the evaluation of patients who have suspected lumbar spinal stenosis. In patients who have axon loss root disease resulting from lumbar canal stenosis, nerve conduction studies may reveal reduced amplitude of motor evoked responses recorded from the small foot muscles after stimulating the peroneal and tibial nerves, with little or no change in conduction velocities or distal latencies [13]. Sensory amplitudes recording from the superficial and sural nerves generally are expected to be unaffected, because the pathology of the nerve roots in lumbar spinal stenosis is at a preganglionic level. In rare instances, the L5 sensory ganglia have an intraspinal location and, therefore, may be involved in nerve root compressive disorders localized to the lateral recesses, causing attenuation of the superficial peroneal sensory amplitudes [18]. It also should be recalled that sensory responses in the lower extremities may be reduced or absent, because the age range of patients affected with lumbar spinal stenosis overlaps with the age when sensory responses are lost as part of normal aging. H-reflexes commonly are attenuated or absent, and, in instances when the sural response is preserved, this finding is all the more suggestive of preganglionic S1 root dysfunction [13]. Peroneal and tibial F-wave chronodispersion (the difference between the shortest and longest F latencies in a series of F waves) [19] may be increased abnormally after 3 minutes of standing [20].

The needle electrode examination is considered the single most useful diagnostic method in the electrophysiologic evaluation of patients who have suspected nerve root compromise in the setting of lumbar spinal stenosis [13]. In the older population most at risk for this condition, a painful, positive straight leg raising radiculopathy is encountered in few individuals [21], and, therefore, needle electrode examination features of single root lesions are uncommon. Patients presenting with lumbar spinal stenosis, especially those who are elderly, are much more likely to experience compressive effects on the cauda equina and, therefore, may manifest EMG changes typical of multiple root involvement [21]. Wilbourn and Aminoff [13] described bilateral, multiple lumbosacral radiculopathies in approximately half of patients who have lumbar spinal stenosis, with L5 and S1 roots involved most commonly. In many patients, especially those who have lesser degrees of lumbar spinal stenosis and accordingly less compression of the cauda equina, the needle examination may be only mildly abnormal or within normal limits. When present, needle electrode examination abnormalities typically are noted in the categories of spontaneous activity and motor unit potential morphology. Because of the chronicity of lumbar spinal stenosis, there is an opportunity for motor unit reinnervation; therefore, fibrillation potentials tend to be restricted to the distal muscles of the myotomes, and motor unit potentials have attributes of chronic neurogenic change, such as prolonged duration and increased amplitude [13].

Finally, electrodiagnostic studies also are helpful in identifying common disorders that might coexist with lumbar spinal stenosis. For example, they detect peripheral nerve involvement in the setting of diabetes (reduced or absent sensory and motor amplitudes in the lower and upper extremities, along with mild slowing of nerve conduction velocities), a condition that might lead to sensory symptoms in the legs and discomfort in the buttocks and legs. Diabetic polyneuropathy often is a complex and multifaceted disorder with features of polyneuropathy and polyradiculopathy, potentially simulating some of the clinical features of lumbar spinal stenosis [15].

The exercise treadmill test—wherein the ability of patients to walk is quantified and any difficulty in walking is characterized fully (determining if the limitation on walking is secondary to neurogenic claudication or some other cause [eg, dyspnea])—plays an important role in the diagnostic process in patients suspected of having lumbar spinal stenosis [22]. In a group of 29 patients who had mild lumbar spinal stenosis, the subset with neurogenic claudication (16/29) covered a significantly shorter distance and the time spent walking was significantly shorter than in the subset with lumbar spinal stenosis without neurogenic claudication and in two control groups (healthy controls and diabetic patients).

  • Differential diagnosis

The most common manifestations of lumbar spinal stenosis include low back and leg pain, numbness and tingling, and neurogenic claudication. Because low back pain typically is an initial and predominating feature of lumbar spinal stenosis, one approach to the evaluation of patients suspected of having lumbar spinal stenosis is to use back pain as the point of departure for the process of differential diagnosis and ask what other conditions present with low back pain and can mimic lumbar spinal stenosis. These conditions must be ruled out before a diagnosis of lumbar spinal stenosis can be established with certainty.

The differential diagnosis of lumbar spinal stenosis, therefore, may be viewed through the lens of the differential diagnosis of low back pain and may be divided into three major categories [11]: mechanical (97% of patients), nonmechanical (1%), and back pain stemming from visceral disease (2%). The first category includes lumbar strain or idiopathic low back pain, which makes up 70% of this group and is distinguished from lumbar spinal stenosis by the lack of neurogenic claudication, relatively normal spinal canal dimensions, and normal electrodiagnostic studies. Other conditions include age-related degenerative disease of the disk and facet joints (10%), frank disk herniations with nerve root compromise (4%), osteoporotic compression fractures (4%), and spondylolisthesis (2%), all of which may present with low back pain but have a distinctive EMG signature (in the case of radiculopathy) or defining neuroimaging characteristics. Nonmechanical spinal conditions include neoplastic and benign cystic lesions of the conus medullaris and cauda equina, infectious diseases (most importantly spinal epidural abscess), inflammatory arachnoiditis, and inflammatory arthropathies. Although not an arthropathy per se, polymyalgia rheumatica deserves mention as a related rheumatologic disorder whose presentation with bilateral aching in the buttocks associated with stiffness in the back might suggest lumbar spinal stenosis until the marked elevation of the erythrocyte sedimentation rate reveals its true character [23]. Visceral diseases include renal diseases (such as nephrolithiasis, pyelonephritis, and perinephric abscess), diseases of the pelvic organs (such as prostatitis, endometriosis, and chronic pelvic inflammatory disease), gastrointestinal diseases (such as pancreatitis, cholecystitis, and penetrating ulcer), and aortic aneurysms. Abdominal and pelvic imaging techniques in concert with routine clinical chemistry and hematologic testing are helpful in identifying nonmechanical and visceral sources of back pain.

In addition to back pain, leg numbness and tingling also are common presenting manifestations of lumbar spinal stenosis. A common cause of such sensory symptoms is polyneuropathy, often associated with diabetes.

  • Management

There are several prospective, long-term, observational follow-up studies that attempt to evaluate conservative versus surgical treatment outcomes for patients who have lumbar spinal stenosis. Amundsen and colleagues [24] compared conservative and surgical management in a cohort of 100 patients who had symptomatic lumbar spinal stenosis, selecting 19 patients who had severe symptoms for surgical treatment and 50 patients who had moderate symptoms for conservative treatment and randomizing 31 patients between the two treatment modalities (18, conservative; 13, surgical). After 4 years, excellent or fair results were found in half of the conservatively managed patients and 80% of the surgically treated group. Although the outcome after 10 years was most favorable for the surgically treated group, the investigators pointed out that an initial conservative approach seems advisable for many patients, because those who have initial unsatisfactory results still can be offered surgery with a good outcome at a later date.

Atlas and colleagues [25], [26] reported on results of a prospective cohort study of surgical or conservative treatment of patients who had lumbar spinal stenosis recruited from the practices of orthopedic surgeons and neurosurgeons throughout Maine, designated the Maine Lumbar Spine Study. Of 148 patients enrolled initially, 4-year outcome measures (level of low back pain, leg pain, and the predominant symptom in the week immediately preceding the evaluation, rated as better, the same, or worse; and degree of patient satisfaction) were available on 119 patients (67 treated surgically and 52 treated nonsurgically) [25]. The surgically treated patients had more severe symptoms and worse functional status at baseline and better outcomes at 4-year evaluation than the nonsurgically treated group, even after adjustment for differences in baseline characteristics. The relative benefit of surgery declined over time but remained superior to nonsurgical treatment. In a second report of the Maine Lumbar Spine Study, Atlas and colleagues [26] reported on the evaluation of 105 patients still alive 10 years after enrollment. After 8 to 10 years, a similar percentage of surgical and nonsurgical patients reported that their low back pain was improved, their predominant symptom improved, and they were satisfied with their current status, although leg pain relief and back-related functional status continued to favor those treated surgically. The investigators concluded by noting that over time it is likely that symptoms of lumbar spinal stenosis will remain stable, and, therefore, for patients who have any trepidation about surgery, conservative management seems appropriate, because long-term outcomes are similar irrespective of treatment modality [26].

Deciding on the most appropriate program of management for a given patient (whether or not to treat conservatively or surgically, the timing of surgery, and which procedure to select) remains a complex decision-making process that requires factoring in the severity of a patient’s symptoms, general medical condition, tolerance for anesthesia, and personal preferences for treatment options. Furthermore, lumbar spinal stenosis is a degenerative condition that does not necessarily worsen with time but has periodic exacerbations and remittances [25]. Johnsson and colleagues [27] described the clinical course of 32 untreated patients who had lumbar spinal stenosis observed over a mean of 49 years. The mean age was 60 years, all had back pain, 75% had neurogenic claudication, all had myelographically defined lumbar canal stenosis, and 30 had EMG abnormalities typical of nerve root involvement. The patients in this study had not undergone surgery because their medical conditions qualified as contraindications or because they refused surgery. At follow-up, patients were evaluated by questionnaire and asked to compare their situation before myelography with their present status, specifically with regard to their walking capacity and their level of pain. Seventy percent of the cases were unchanged, 15% showed improvement, and 15% worsened.

In light of this report and the observation that surgical intervention may be associated with significant increased morbidity, surgical complications, and mortality [8], it seems appropriate to offer conservative management to patients experiencing mild to moderate symptoms when symptoms are not progressive and when work and leisure activities are not hampered seriously. Controlled trials examining the outcome of conservative management, however, are lacking [6].

Several conservative interventions can be considered. Physical therapy can provide gentle back and leg strengthening exercises and mobility training that can reduce the risk of falling. Exercises may include use of an exercise bicycle and brief walks (encouraging walking with a rolling walker to promote a pain-alleviating flexed posture). In addition, patients should avoid lumbar extension exercises, consider the occasional use of lumbar bracing, and adopt a weight loss program if obese. Other treatments of unproved or anecdotal value include medications, such as nonsteroidal anti-inflammatory drugs and muscle relaxants, transcutaneous nerve stimulation and ultrasound therapy, and periodic courses of epidural corticosteroid injections. Delport and colleagues [28] conducted a retrospective review of 140 patients over age 55 who had lumbar spinal stenosis and who had received epidural corticosteroid injections, transforaminally or caudally and under fluoroscopic guidance. The injections provided approximately one third of patients with more than 2 months of relief and more than 50% of patients with improvement in function. Fluoroscopic guidance seems necessary to ensure proper placement of the injecting needle in the epidural space, specifically in the neighborhood of the desired nerve roots.

For some individuals, conservative measures fail to provide adequate relief from severe symptoms of neurogenic claudication that may reach the point of compromising quality of life. In such cases, it is appropriate to consider surgical intervention, even in the geriatric population, to improve walking tolerance and ease disabling leg and back pain [5], [7], [15]. Although widely agreed on validated indications for surgery do not exist (surgical emergencies, however, such as rapidly progressive cauda equina syndrome, are rare) [7]. Good to excellent results of surgery are reported on average in 64% of cases [29], but the range in the published literature is 24% to 100% and there is a great deal of heterogeneity among studies with regard to patient population, patient selection, and outcome measures [7]; the studies are observational and nonrandomized [26]; and surgical techniques are varied [15]. Surgical options include multilevel decompressive laminectomies (because canal stenosis occurs commonly over several levels), unilateral decompressive hemilaminectomy, and multilevel laminotomies, whereby fenestrations are created by removing portions of the lamina of adjacent involved vertebrae, preserving spinous processes, and sparing interspinous ligaments. The goals of surgical intervention are pain relief, increased mobility, preservation of neural tissue, and prevention of increasing clinical deficits [30]. Goals for successful operations include decompression of affected structures (the extent of which depends on the exact location of the stenosis: central canal or lateral recesses or both) and the maintenance of spinal stability postoperatively (usually achieved by preserving facet joint integrity and protecting the pars interarticularis). Spinal fusion becomes necessary to maintain spinal stability during multilevel procedures, when facet joint and pars integrity cannot be preserved. In a systematic review of preoperative predictors for postoperative clinical outcome (level of pain) in lumbar spinal stenosis, depression, coexisting cardiovascular comorbidity, poor walking (resulting from joint athritis, neurologic disease, cardiopulmonary disease), and scoliosis predict poorer subjective outcome (worse postoperative pain). Better subjective outcome is predicted by factors, such as better walking ability, self-rated health, higher income, less coexisting disease, and pronounced central stenosis [31].

In the special case of the management of spinal stenosis in Paget’s disease, treatment of this complex metabolic bone disorder is multifaceted. Typically it begins with antipagetic medical therapy, including bisphosphonates, calcitonin, and mithramycin, which often is successful in improving or reversing the clinical symptoms of lumbar spinal stenosis [17]. Surgical decompression of spinal stenosis may be necessary should there be failure of medical treatment and is best tailored to the pathology causing neural compression.


References

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[19] Fisher MA. Electrophysiology of radiculopathies. Clin Neurophysiol. 2002;113:317–335.

[20] Tang LM, Schwartz MS, Swash M. Postural effects on F wave parameters in lumbosacral root compression and canal stenosis. Brain. 1988;207:207–213.

[21] Levin KH. Electrodiagnostic approach to the patient with suspected radiculopathy. Neurol Clin. 2002;20:397–421.

[22] Adamova B, Sohanka S, Dusek L. Differential diagnostics in patients with mild lumbar spinal stenosis: the contributions and limits of various tests. Eur Spine J. 2003;12:190–196.

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Responses

  1. Clear and informative – I asume it is factually accurate

  2. Conservative therapies (physical therapy, medications, steroidal injections) may be attempted first to limit inflammation and control pain, but these will not address the underlying problem within the spine. Patients with severe neurological deficit or pain that is not relieved through non-operative treatments may be eligible for spinal stenosis surgery.


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